Triptolide is widely used in the clinical treatment of various diseases. Side effects, including reproductive toxicity to male patients, limit its application. However, no detailed mechanisms or potential intervention targets have been reported. In this study, we show that triptolide activated the mitochondrial apoptosis pathway in rat testicular Leydig cells and induced apoptosis both and , which may cause hypoleydigism and impair spermatogenesis. Mechanistically, triptolide-induced dynamin-related protein 1 (Drp1) overexpression, which interfered with mitochondrial dynamic stability to activate the mitochondrial apoptosis pathway. Mdivi-1, a selective Drp1 inhibitor, partially reversed the mitochondrial dynamic disturbance and rat testicular Leydig cell apoptosis induced by triptolide. Inhibiting Drp1 over-activation may be a new strategy for mitigating the reproductive toxicity of triptolide.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7985071PMC
http://dx.doi.org/10.3389/fphar.2021.616803DOI Listing

Publication Analysis

Top Keywords

leydig cell
8
cell apoptosis
8
reproductive toxicity
8
mitochondrial apoptosis
8
apoptosis pathway
8
rat testicular
8
testicular leydig
8
mitochondrial dynamic
8
triptolide
5
apoptosis
5

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!